SPECIFIC AIMS: Approximately 50% of hypertensive patients exhibit changes in blood pressure in response to changes in salt intake, referred to as salt-sensitive hypertension.1 We hypothesize that a population of patients with salt-sensitive hypertension has mutations within the epithelial sodium channel that result in a gain of function and hypertension. Recent DNA analysis of patients with an extreme form of salt-sensitive hypertension known as Liddle's syndrome has revealed mutations of the epithelial sodium channel.2,3 These mutations lead to an increase in channel function, presumably allowing for an abnormally high reabsorption of sodium through this ion channel within the distal convoluted tubules of the kidney, causing hypertension. The specific aim of this proposal is to determine if a population of patients with salt-sensitive hypertension have mutations within the epithelial sodium channel that are associated with hypertension. The control group will be those patients with salt-resistant hypertension.